Heart failure usmle

Heart failure usmle DEFAULT

Continuing Education Activity

High-output cardiac failure is a less common form of heart failure, and although it may sound contradictory at first, in the simplest form, it is still the heart's inability to provide sufficient blood for the body's demand. Most patients with heart failure are either classified as a systolic or diastolic dysfunction with increased systemic vascular resistance, however, patients with high output cardiac failure have normal cardiac function and decreased systemic vascular resistance, either secondary to diffuse arteriolar dilation or possible bypass of the arterioles and capillary beds, leading to activation of neurohormones. This activity reviews the cause, pathophysiology, and presentation of high output heart failure and stresses the role of the interprofessional team in its management.


  • Review the causes of high output failure.
  • Describe the presentation of high output heart failure.
  • Summarize the treatment options for high output failure.
  • Explain modalities to improve care coordination among interprofessional team members in order to improve outcomes for patients affected by high output heart failure.


High-output cardiac failure is a less common form of heart failure, and although it may sound contradictory at first, in the simplest form, it is still the heart's inability to provide sufficient blood for the body’s demand.[1][2][3][4] Most patients with heart failure are either classified as a systolic or diastolic dysfunction with increased systemic vascular resistance, however, patients with high output cardiac failure have normal cardiac function and decreased systemic vascular resistance, either secondary to diffuse arteriolar dilation or possible bypass of the arterioles and capillary beds, leading to activation of neurohormones.[3][4] The problem lies with an increase in the body’s demand for perfusion that the heart is not able to provide, even with a normal cardiac function. In terms of cardiac output, a high cardiac output state is defined as a resting cardiac output greater than 8 L/min or a cardiac index of greater than 4.0/min/m2 [1], and heart failure occurs when that cardiac output is insufficient to supply the demand. High-output cardiac failure is more of a consequence of an underlying disease process. The underlying etiology of this type of cardiac failure largely dictates the presenting symptoms and signs, evaluation, and treatment.


Causes of high-output cardiac failure can be simplified into two main categories: (1) there is an increase in the body’s demand for blood from increased metabolism or (2) there is a bypass of the arteriolar and capillary bed causing an increased flow into venous circulation from a lack of resistance, leading to increased oxygen consumption and a low systemic vascular resistance, respectively.[1][2] These processes both lead to an increase in cardiac output, either by cardiac remodeling or tachycardia and chronic plasma volume overload. Etiologies can further be characterized as metabolic, myocardial, mechanical vascular, or a combination of these. A single study conducted by Reddy et al. studied the etiologies of high-output cardiac failure, reporting common causes of obesity (31%), liver disease (23%), arteriovenous shunts (23%), lung disease (16%), and myeloproliferative disorders (8%).[1]


Several specific metabolic disease processes can increase metabolic demand, causing an increase in cardiac output.

Hyperthyroidism causes an increase in thyroid hormone affecting both the cardiac and systemic tissue.[5] Cardiac effects of thyroid hormone eventually lead to increased contractility and heart rate, while increased systemic metabolism leads to the creation of increased cellular waste products, causing a reduction in systemic vascular resistance.[5][6] Untreated, hypercontractility, tachycardia, and volume overload lead to the development of cardiomyopathy and hypertrophy.[7]

Myeloproliferative disorders also have been associated with high-output cardiac failure. They are linked to increased cellular metabolism and high cell turnover.[1] This causes a state of increased metabolic demand and decreased systemic vascular resistance, leading down a path to high-output cardiac failure if there are no intervention mechanisms such as those discussed in pathophysiology.[1]


Myocardial etiologies largely reflect diseases that have a direct myocardial effect but generally have multifactorial pathophysiology involving metabolic and vascular effects as well. An example of this is hyperthyroidism, where thyroid hormones have a global effect including a direct effect on myocardial tissue.

Sepsis causes a global inflammatory response to an infection, causing a wide range of hemodynamic changes and phases.[2][8] Patients usually present with an initial hypovolemic phase requiring volume resuscitation, however afterward, patients are in a hyperdynamic phase with high cardiac output and a low systemic vascular resistance consistent with high-output cardiac failure.[8] This is largely driven by inflammatory cytokines, causing a systemic vasodilatory effect in the setting of adequate myocardial function; however, subsequent phases of sepsis usually lead to depression in myocardial function.[2][8]

Thiamine is an essential vitamin used in the formation of thiamine pyrophosphate, an essential cofactor used in metabolism for energy production. Severe thiamine deficiency causes beriberi, which results from a buildup of pyruvate and lactate in the blood that leads to systemic vasodilation. Additionally, Ikram published a case series regarding cardiac beriberi showing that thiamine deficiency affects cardiac myocytes directly and describing vacuolation and intercellular edema with myofiber hypertrophy, fibrosis, and cellular infiltration in histopathology.[9] This causes an increased venous return and thus a high cardiac output, eventually leading to cardiomyopathy. If left untreated, symptoms of heart failure suggesting a decompensated state become evident.

Chronic lung disease is associated with high-output cardiac failure, largely with right-sided heart failure. Chronic hypoxia and hypercapnia drive a reduced systemic arterial resistance, leading to chronic volume overload, while pulmonary vascular constriction causes increased right heart remodeling; the left heart remains largely functional and produces a high cardiac output.[1]

Peripheral Vascular Effects

These effects are largely due to the bypass of the arteriolar and capillary bed, leading to increased direct flow into venous circulation. In the systemic vascular system, the majority of resistance is in the arteriolar system, considering the collective decrease in radius among all of the arterioles and thus decreasing flow into the venous circulation. If the arteriolar system is bypassed, flow increases to the venous circulation causing an increased venous return to the heart, eventually leading to cardiac volume overload.

Arteriovenous fistulas (AVF), either congenital or acquired, cause a shunt from an artery to a vein, bypassing the resistance of the arteriolar and capillary system. This causes an increased flow of blood to the heart, requiring an increase in heart rate and stroke volume, leading to increased cardiac output.[1] Congenital etiologies involve the formation of large or numerous hemangiomas or telangiectasias. Acquired etiologies include traumatic, iatrogenic formation (eg, puncture wounds, AVF formation for hemodialysis, transjugular intrahepatic portosystemic shunting procedure, arterial puncture for catheterization) or development of skeletal disorders causing several, minute AVF formations in response to extensive bone turnover.[10][11]

Liver cirrhosis is associated with arteriovenous shunts and decreased systemic vascular resistance.[1] Mechanisms of impaired clearance of vasoactive substances and bacterial translocation have been described as the driving force for decreased systemic vascular resistance.[11][12][13] This decrease in systemic vascular resistance is so severe that the increase in cardiac output is not sufficient, leading to a decompensated high-output cardiac failure.

The mechanism for obesity as an etiology is not well defined; however, it is associated with excessive vasodilation. Mechanisms of reduced arterial resistance secondary to vasoactive adipokines have been described in the literature.[14] Obesity also has a direct effect on cardiac function by alternating myocardial metabolism due to increased insulin resistance.[15] It has been shown in animal models that increased fatty-acid oxidation in cardiac myocytes can lead to left ventricular dysfunction; however, exact mechanisms are unknown.[15] 

Other etiologies that are less defined but mentioned in the literature include erythroderma, carcinoid syndrome, mitochondrial diseases, acromegaly, and Paget disease of bone. Stress, exercise, fever, and pregnancy are all contributors; however, they are not defined as direct causes of high-output cardiac failure.


Heart failure is very common. It is stated to be the cause of millions of office visits per year and is the most common diagnosis of hospitalized patients. In the United States, it is published that more than 500,000 new cases are diagnosed per year, and the current prevalence is about 5 million.[16] This includes all forms of heart failure, including systolic and diastolic dysfunction as well as high-output cardiac failure. However, isolated high-output cardiac failure is a far less common form of heart failure, and the exact incidence and prevalence rates are not known.[1] This may be because high-output cardiac failure is secondary to other underlying pathologies and may or may not be identified appropriately. Furthermore, the prevalence and incidence of high-output cardiac failure are likely related to conditions that result in a high-output state.


The pathophysiology of high-output cardiac failure is largely unique to the underlying etiology. However, they all are characterized by having a low systemic vascular resistance, decreased arterial-venous oxygen gradient, and an elevated cardiac output. The latter is somewhat confusing, but even in the setting of an elevated cardiac output, the output is not sufficient to the body’s required demand, leading to clinical heart failure. The decreased supply of blood causes similar neurohormonal alterations seen in other causes of heart failure, with activation of the renin-angiotensin-aldosterone system (RAAS), adrenergic nervous system, and an excess of antidiuretic hormone. These systems are in place to increase intravascular blood volume in acute and subacute settings. However, chronic activations cause a progressive decline in cardiac function. Simply, in an attempt to compensate for hemodynamic burdens, the heart undergoes hypertrophy and remodeling to maintain contractility and reduction of wall stress by dilatation. Over time, the dilatation exceeds and holds more volume of blood that can be effectively pumped, causing heart failure.[1]

The goal of the adrenergic system is to increase cardiac output, which in high-output cardiac failure is already elevated, by increasing contractility (i.e., stroke volume) and heart rate while maintaining systemic blood pressure by causing vasoconstriction. Activated by baroreceptors in the carotid sinus and aortic arch, a decrease in transmission by these receptors in response to low blood pressure causes an increase in sympathetic stimulation. This attributes to ventricular hypertrophy and cardiac remodeling.[1]

The RAAS is activated by an increase in renin in response to decreased renal artery perfusion and the adrenergic nervous system. The release of renin leads to increased circulating angiotensin II, causing an increase in aldosterone secretion from the adrenal cortex and stimulating thirst in the hypothalamus. Aldosterone increases sodium reabsorption, causing increased water retention at the level of the kidneys in attempts to increase intravascular volume and thereby augmenting preload. An increase in preload allows for increased cardiac output via the Frank-Starling mechanism; however, in an already weak heart, this mechanism does not augment cardiac output as much as it causes excessive hypervolemia, leading to peripheral edema and pulmonary congestion seen in clinical heart failure.

Antidiuretic hormone (ADH) is activated in response to angiotensin II and baroreceptors, causing an increase in water retention at the level of the kidneys. Additionally, the antidiuretic hormone can contribute to vasoconstriction as well.

History and Physical

As with any initial evaluation, a thorough history and physical is paramount. In patients with high-output cardiac failure, history regarding chronic medical conditions can facilitate in determining the underlying etiology of high output cardiac failure.[1] Similar to other forms of heart failure, patients can present with complaints of progressively worsening fatigue, swelling, or dyspnea, either at rest or exertion, that is classically positional and worse when supine. Some may present with complaints of palpitation or heart racing as well. On physical exam, tachycardia, pulmonary and peripheral edema, and jugular venous distention can present. Contrasting to other forms of heart failure, in high-output cardiac failure, patients have a wide pulse-pressure and warm extremities secondary to a low systemic vascular resistance. The cardiac examination would be most notable for, if present, a bounding point of maximal impulse, systolic flow murmurs, and additional heart sounds S3 or even an S4. S3 sounds are secondary to blood filling a compliant ventricle from passive filling, which is heard in early diastole. S4 sounds are secondary to blood filling a noncompliant ventricle from atrial contraction, which is heard in late diastole and may be findings in heart failure that has progressed.

Further physical signs are related to the underlying etiologies. At times, the cardiac symptoms of high-output cardiac failure are secondary and somewhat incidental, as patients come with presenting symptoms of the underlying disease.

Hyperthyroidism presents with a wide range of symptoms. Relative to the heart, patients can present with tachycardia, palpitations, and dyspnea from hyperthyroidism alone, even in the absence of high output cardiac failure. Physical exam findings can include fever, eyelid retraction and lid lag, tremor, hyperreflexia, hyperactivity, enlarged thyroid gland with possible tenderness, and exophthalmos with periorbital edema in addition to cardiac findings.

Myeloproliferative disorders can show a wide range of findings in addition to cardiac findings. Fever, fatigue, dyspnea, increased bleeding episodes (e.g., epistaxis, bruising), with signs of splenomegaly and peripheral blood smear abnormality specific to the myeloproliferative disorder.

Sepsis presents on a wide spectrum, from fever, chills, fatigue, loss of appetite, palpitations to altered mentation, and even coma secondary to acute systemic vasodilation. A physical exam can show fever, tachycardia, tachypnea, and warm extremities in the first presenting stages of sepsis with further symptoms, depending on the source of infection. Further stages of sepsis can cause a worsening myocardial dysfunction, eventually leading to a left ventricular failure and causing systolic heart failure.

Berberi usually presents with a history of a malnourished, alcoholic, dieting, or bariatric patient. Patient presentation depends on the form of beriberi, characterized by either dry or wet beriberi. Relative to the heart, dry beriberi is separated from wet beriberi by symptoms of heart failure. Patients often present with complaints of dyspnea, orthopnea, palpitations, and peripheral swelling, with respective physical exam findings of clinical heart failure. Additional signs of beriberi are burning pain in the extremities, muscle weakness, and possible fall secondary to peripheral neuropathy with both sensory and motor involvement.

Chronic lung disease usually involves a patient with a smoking history, who has already been diagnosed with progressive lung disease; however, chronic lung disease can be diagnosed on initial presentation of worsening dyspnea, cough, and wheezing. Relative to the heart, when patients have chronic lung disease it often results in right-sided heart failure secondary to pulmonary hypertension. Isolated right-sided heart failure can lead to clinical symptoms and signs of peripheral swelling with pitting edema, positive jugular venous distention, parasternal heave, fixed split S2, and possible S3 or S4 heart sound.

Arteriovenous fistulas (AVF) can either be congenital or acquired. Usually, congenital AVF presents with diffuse hemangiomas from childhood (e.g., hereditary hemorrhagic telangiectasia or Osler-Weber-Rendu syndrome) with associated bleeding episodes from mucocutaneous or gastrointestinal sources. Acquired AVFs can be iatrogenic or traumatic with the respective history. Often, acquired iatrogenic AVFs are formed intentionally for hemodialysis access or secondary to a complication. All of these, if causing high-output cardiac failure, cause symptoms of progressive dyspnea, orthopnea, and swelling, with respective physical exam findings of heart failure. Patients with AVFs, especially for heart disease access, also have findings of palpable thrills and audible bruits over the AVF itself.

Patients with liver cirrhosis present with a wide spectrum of symptoms. History is notable for causes of liver cirrhosis if already diagnosed, such as alcohol abuse, viral hepatitis, obesity, autoimmune disease to name a few. Initial symptoms of the presentation can be very nonspecific to symptoms of decompensated liver disease. Fatigue, weakness, generalized unwellness, increased swelling, dyspnea, abdominal distention, yellowing of skin and eyes, confusion, and even gastrointestinal bleeding can be presenting symptoms. Physical exam findings are just as variable in liver cirrhosis and highly dependent on the severity of liver disease and if in a decompensated state. Relative to the heart, patients have physical exam findings of clinical heart failure in addition to decompensated liver cirrhosis.

Patients with obesity have a high body mass index (BMI), defined as a BMI greater than or equal to 30 kg/m2, with severe obesity indicated by a BMI of greater than or equal to 40 kg/m2. A physical exam is largely specific to, as well as limited by, an obese habitus. Relative to the heart, physical exam findings of clinical heart failure with tachycardia may be evident.


The diagnostic evaluation for high-output cardiac failure is important, but determining the underlying etiology is paramount as management changes. The first step in diagnosing heart failure is based on the initial history and physical. Aside from the history and physical exam, initial laboratory testing and imaging should be obtained. The use of natriuretic peptide levels is highly beneficial when the diagnosis of heart failure is not clear, with elevated levels suggesting heart failure. Electrocardiogram and a transthoracic echocardiogram also should be obtained. Findings of clinical heart failure in the setting of a high output cardiac state give the diagnosis of high-output cardiac failure. In contrast to other forms of heart failure, high-output cardiac failure has the presence of high cardiac output and/or cardiac index.[1]

The final step in evaluation is to determine the cause of high-output cardiac failure. Depending on the initial presentation and physical exam, diagnostic studies will differ. The history and physical will strongly dictate which further testing is necessary.

Treatment / Management

Management begins with the acute intervention of heart failure. Depending on the severity, treatment should be directed towards acute respiratory failure from volume overload and hypotension if present. The initial management can range from intermittent diuretic therapy and oxygen supplementation to continuous diuretic infusion, non-invasive positive pressure ventilation, or intubation. If hypotension and decreased organ perfusion are evident, inotropic medications are warranted. Once patients are stabilized and are no longer in a decompensated state, management can be directed at the underlying etiology. The treatment for specific etiologies is only briefly described further.

Treatment of hyperthyroidism is focused on symptomatic therapy with the goal to decrease the circulating thyroid hormones, either by medications and/or the use of radiotherapy or surgery if necessary. Myeloproliferative diseases are treated according to the specific underlying disease and may involve hematopoietic cell transplantation depending on the severity. Treatment is largely variable, depending on the disease and severity of symptoms. Sepsis treatment is guided by the Surviving Sepsis Campaign guidelines and involves early recognition, immediate and aggressive intravenous fluid resuscitation, and antibiotic therapy with an investigation to determine the source of infection. Thiamine deficiency causing beriberi is treated with thiamine replacement for a minimum of 2 weeks. Chronic lung disease is a progressive disease with treatment catered to the underlying pulmonary disease. In general, hypoxia and hypercapnia are addressed, and management is symptomatic therapy and slowing the progression of the underlying disease. Acquired AVFs are treated with either closure or reduction of blood flow. It is more pertinent in patients on hemodialysis, who need access; however, if presenting with high-output cardiac failure, it may be necessary to close, and alternative access sites should be obtained. Treatment of congenital AVFs can involve medical therapy, invasive embolization, or surgical excision, depending on the exact cause. Liver cirrhosis that is advanced enough to cause high-output cardiac failure is end-stage and treatment involves liver transplantation. Medical therapy has a role in fluid management for hypervolemia, involving the use of combined loop diuretics and anti-mineralocorticoids, which may limit the flow through shunts.

Differential Diagnosis

Clinical heart failure is a diagnosis based on a patient's history and physical on initial assessment. Though the type may not be clear, most patients present very similarly, if not the same. Hypervolemia, dyspnea on rest or exertion, orthopnea, and fatigue are the general symptoms of heart failure. Different types of heart failure include heart failure with reduced ejection fraction and heart failure with preserved ejection fraction and can be differentiated from high-output cardiac failure by measuring the cardiac output and/or cardiac index and low systemic vascular resistance.


The prognosis of high-output cardiac failure is dependent on the cause of the condition. As referenced above, Reddy published a retrospective analysis of patients with high-output cardiac failure, reporting an increased 3-mortality rate compared to the control group (subjects free of heart failure). The study reports a hazard ratio of 3.4 (1.6 to 7.6). The study further stated that among patients with high-output cardiac failure, causes related to obesity had the lowest 5-year mortality at 19%, compared to liver disease (58%), and heart failure associated with shunt formation (59%) which carried the highest 5-year mortality.[1]

Enhancing Healthcare Team Outcomes

Generally, in heart failure, the heart is weak and cannot appropriately provide sufficient blood to the body. If severe enough, patients can present with cardiogenic shock, and hallmark presentation is increased systemic peripheral resistance secondary to the body’s attempt to allow adequate perfusion. High output cardiac failure presents as clinical heart failure, however with a decreased systemic vascular resistance. Several different etiologies can lead to this condition and each requires a different therapy and management plan. The healthcare team should be prepared for management strategies in evaluating and treating patients with this condition. [Level 5]



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Sours: https://www.statpearls.com/ArticleLibrary/viewarticle/22873

Continuing Education Activity

Heart failure (HF) is a common and potentially fatal disease if left untreated. This article aims to describe the different types of heart failure. It also describes the stages, types of HF, and how it is diagnosed and treated. It also highlights the role of interprofessional approach involving patients, physicians, nurses, families, and caretakers.


  • Describe the different types and stages of heart failure.
  • Identify the etiologies and epidemiology of heart failure.
  • Explain the clinical signs and symptoms of heart failure. Review the evaluation and diagnostic
  • Outline the importance of interprofessional and an interprofessional team to improve outcomes and enhance the delivery of care in patients affected by heart failure.


Heart failure (HF) is a complex clinical syndrome that results from either functional or structural impairment of ventricles resulting in symptomatic left ventricle (LV) dysfunction. The symptoms come from an inadequate cardiac output, failing to keep up with the metabolic demands of the body. It is a leading cause of cardiovascular morbidity and mortality worldwide despite the advances in therapies and prevention. It can result from disorders of the pericardium, myocardium, endocardium, heart valves, great vessels, or some metabolic abnormalities.


Three main phenotypes describe HF according to the measurement of the left ventricle ejection fraction (EF), and the differentiation between these types is important due to different demographics, co-morbidities, and response to therapies:

  • Heart failure with reduced ejection fraction (HFrEF): EF less than or equal to 40%
  • Heart failure with preserved EF (HFpEF): EF is greater than or equal to 50%
  • Heart failure with mid-range EF (HFmrEF) (other names are: HFpEF-borderline and HFpEF-improved when EF in HFrEF improves to greater than 40%): EF is 41% to 49% per European guidelines and 40 to 49% per the US guidelines.[1][2] A new class of HF that introduced by the 2016 European Society of Cardiology (ESC) guidelines for diagnosis and management of HF. This class was known as the grey area between the HFpEF and HFrEF and now has its distinct entity by giving it a name as HFmrEF.

All patients with HFrEF have concomitant diastolic dysfunction; in contrast, diastolic dysfunction may occur in the absence of systolic dysfunction.


Multiple conditions can cause HF, including systemic diseases, a wide range of cardiac conditions, and some hereditary defects. Etiologies of HF vary between high-income and developing countries, and patients may have mixed etiologies.[3] Ischemic heart disease and chronic obstructive pulmonary disease (COPD) are the most common underlying causes of HF in high-income regions. Conversely, hypertensive heart disease, rheumatic heart disease, cardiomyopathy, and myocarditis are the primary conditions for HF in low-income regions, according to a systemic analysis for the Global Burden of Disease Study.[4] More than two-thirds of all cases of HF are attributable to ischemic heart disease, COPD, hypertensive heart disease, and rheumatic heart disease. 

  • Coronary artery disease (CAD): chronic and acute ischemia causes direct damage to the myocardium and leads to remodeling and scar formation, resulting in inadequate relaxation in diastole and impaired contraction in systole, which decreases contractility and cardiac output (CO). This scar formation may also correlate with aneurysm formation, and that further impairs contractile performance and relaxation. Myocardial infarction (MI) also causes dyssynchronous contraction of the infarcted segment, subsequent remodeling of the ventricle, ventricular dilatation with annular dilation, and mitral regurgitation that predispose to HF and decrease the CO. Several tachyarrhythmias such as atrial fibrillation/atrial flutter or non sustained ventricular tachycardia is common in patients with CAD and can deteriorate the cardiac function more. More than 70% of cases with HF have CAD.[5] CAD is a strong predictor of mortality in patients with acute HF. However, the role of coronary revascularization in reducing HF-related morbidity and mortality is still controversial, and viability testing may be useful to select the population that may benefit from revascularization.[6]
  • High blood pressure (HBP): HBP is an independent risk factor for CAD. The high prevalence of HBP makes it a possible cause of HF in around one-fourth to one-third of cases. HBP increases vascular resistance and activates the renin-angiotensin-aldosterone system (RAAS). The heart must pump up blood against a higher afterload caused by HBP, which increases the myocardial mass as a compensatory mechanism to maintain a normal CO and that causes left ventricular hypertrophy (LVH). If blood pressure (BP) remains uncontrolled, apoptosis and fibrosis may result. LVH increases the myocardial stiffness and can cause ischemia, which leads to HFpEF or HFrEF. Control of BP is of paramount importance in improving the prognosis of HF. The Systolic Blood Pressure Intervention Trial (SPRINT) has shown that lowering the systolic BP to a target goal of less than 120 mmHg in HBP patients without diabetes had lower rates of HF with 38% lower relative risk comparing to systolic BP goal of less than140 mmHg.[7]
  • Chronic obstructive pulmonary disease (COPD): COPD increases the risk of CAD and other smoking-related illnesses, cardiac dysrhythmias and can cause pulmonary hypertension and right heart failure. 
  • Valvular heart disease: degenerate valve disease in developed countries and rheumatic valve disease in low-income countries can cause HF. Aortic and pulmonary stenosis increases the ventricular afterload and may cause HF. In valve regurgitation, a persistent volume overload can cause ventricular enlargement and functional impairment that may lead to HF. 
  • Cardiomyopathies (CMP): CMP is a disease in which there are functional and structurally heart muscle abnormalities in the absence of CAD, HBP, valvular, or congenital heart disease. CMP categorizes into five types, which can be genetic or acquired: dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), restrictive cardiomyopathy (RCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), and other unclassified cardiomyopathies (isolated noncompaction of the left ventricle [INLV] and Takotsubo syndrome are also in this category). CMP can cause HFrEF, HFpEF, or HFmrEF.

Other possible causes of HF include congenital heart disease, myocarditis, infiltrative disease, peripartum cardiomyopathy, human immunodeficiency virus (HIV), connective tissue disease, amyloidosis, substance abuse, long-standing alcohol use, obesity, diabetes mellitus (DM), hyperthyroidism (can cause high-output HF), pulmonary hypertension (can cause right HF), constrictive pericarditis (can cause HFpEF), pulmonary embolism (can cause right HF), and chemotherapies (like doxorubicin). 


HF is a significant public health problem with a prevalence of over 5.8 to 6.5 million in the U.S.[8][9] and around 26 million worldwide.[10] The expectation is that 8 million people in the United States will have this condition by 2030, accounting for a 46% increase in prevalence.[11] The prevalence of HF increases with age as per data from Framingham Heart Study that estimated the prevalence of HF to be 8 per 1000 in men at age 50 to 59 years and goes up to 66 per 1000 in men at ages 80 to 89 years, similar values in women (8 and 79 per 1000).[12] At age 45 years, the lifetime risks for HF through age 75 or 95 years were 30% to 42% in white men, 20% to 29% in black men, 32% to 39% in white women, and 24% to 46% in black and higher BP and BMI at all ages led to higher lifetime risks.[13] The increase in HF prevalence does not necessarily have links with an increase in HF incidence. The aging of the population and modern therapies for cardiac patients that led to increase survival could explain the increase in prevalence even with a reduction in the incidence (due to prevention programs and better treatment of acute coronary syndromes).[14] 

Between 13% and 24% of patients with HF have HFmrEF.[15] Between 40% and 60% of patients with HF have diastolic dysfunction, and more than 50% of HF are HFpEF.[16][17] The prevalence of HFpEF is increasing, and researchers expect that by 2020, 65% of patients hospitalized for HF will have HFpEF.[18] Patients with HFpEF are older, more frequently have hypertension, are overweight, and are more commonly women, compared to HFrEF.[19] Risk factors for HFpEF are multifactorial and complex, and there is no known prevention other than the treatment of the risk factors, such as hypertension, diabetes, and obesity; whereas prevention and early treatment strategies (i.e., early revascularization) appear to be effective in reducing the risk and severity of acute myocardial infarction. These observations may explain a reduction in the incidence of HFrEF but an increasing incidence of HFpEF and HFmrEF.


The pathophysiology of HF is complex and includes structural, neurohumoral, cellular, and molecular mechanisms activation to maintain physiologic functioning (maladaptation, myocyte hypertrophy, myocyte death/apoptosis/regeneration, and remodeling).[20] The performance of LV function and stroke volume is under the control of preload (venous return and ventricular end-diastolic volume), myocardial contractility, and afterload (the impedance during ejection from aorta and wall stress). The Frank-Starling curve explains the relationship between stroke volume/cardiac output and left ventricle end-diastolic pressure (LVEDP) or pulmonary capillary wedge pressure (PCWP) in which there is a steep and positive relationship between increased cardiac filling pressures and increased stroke volume/cardiac output. This relationship is right-shifted, representing the decreased contractility, and higher pressure is required to achieve the same cardiac output and flattened in advanced disease, which means that augmentation in venous return and LVEDP fails to increase the stroke volume. (Figure 1) 

HFpEF has the same pathophysiologic processes as HFrEF but in response to increased ventricular stiffness and altered relaxation than CO in HFrEF. This stiffness and altered relaxation cause concentric LVH (instead of eccentric LVH as in HFrEF) and shift the pressure-volume curve to the left.

HF (HFrEF, HFpEF, and HFmrEF) causes activation of neurohumoral systems to maintain perfusion of vital organs: sympathetic nervous systems (SNS), renin-angiotensin-aldosterone system (RAAS), antidiuretic hormone, and other vasoactive substances (brain natriuretic peptide (BNP), nitric oxide, and endothelin). HF causes decrease carotid baroreceptor response, which in turn increases sympathetic nervous activity (SNS) and leads to increase cardiac contractility and heart rate, vasoconstriction, and increased afterload. Activation of RAAS in response to low renal perfusion from HF causes salt/water retention and increases preload. RASS activation increases angiotensin II that leads to vasoconstriction and more salt and water retention, which further stress the ventricular wall and cause dilatation (remodeling) and worsening ventricular function and further HF. Those compensatory mechanisms cause negative remodeling of the heart (inflammation, apoptosis, hypertrophy, and fibrosis) and worsening left ventricular function.

History and Physical

A thorough history and physical exam should be obtained and performed in all patients with suspected HF, as the entire basis of the diagnosis is on clinical symptoms and signs. It also should include assessment of risk factors and possible etiologies of the HF. Symptoms of HF are similar regardless of the EF. Symptoms are more severe with exertion and either secondary to fluid accumulation (dyspnea, orthopnea, edema, and abdominal discomfort from hepatic congestion and ascites in the setting of right heart failure) or due to decreased cardiac output (fatigue, anorexia, and weakness). Other less typical symptoms include nocturnal cough, loss of appetite, wheezing, palpitations, depression, syncope, bendopnea (short of breath while bending forward), and dizziness. In advanced HF, patients may have resting sinus tachycardia, diaphoresis, narrow pulse pressure (less than 25 mmHg due to decreased cardiac output), and peripheral vasoconstriction (cool and pale extremities due to decreased perfusion). Volume overload manifests as peripheral edema (extremities edema, ascites, scrotal edema, and hepatosplenomegaly), elevated jugular venous pressure (JVP), and pulmonary congestion (rales on the exam and pleural effusions). Displaced apical impulse (laterally past the midclavicular line, which is a sign of LV enlargement), parasternal lift (right ventricular enlargement), and an S3 gallop. At each clinic visit, symptoms and signs of HF require assessment to monitor response to therapy and stability over time. It is also important to check vital signs and assess volume status during each clinic visit. 


  • Complete blood count to rule out anemia as a possible cause of patients' symptoms. Besides, anemia is associated with higher HF severity, and intravenous iron replacement is important to improve functional status and quality of life if ferritin under 100 ng/ml or 100 to 300 ng/ml if transferrin saturation is below 20%.[21]
  • Serum electrolytes (including calcium and magnesium levels) and kidney functions (blood urea nitrogen and serum creatinine): serum creatinine and blood urea are prognostic factors in hospitalized patients with HF, and hyponatremia plays a prognostic factor role in chronic patients with HF. Besides, some HF medications can cause electrolyte abnormalities and kidney dysfunction (like spironolactone, angiotensin-converting enzyme inhibitor (ACEi), and furosemide). 
  • Measurement of B-type Natriuretic peptide (BNP) or N-terminal pro-B-type natriuretic peptide (NT-proBNP) is helpful to support the clinical diagnosis of HF in the ambulatory setting and to support the diagnosis of acutely decompensated HF in hospitalized/ER patients. 
  • Other laboratory workups include glucose, fasting lipid profile, liver function tests, and thyroid-stimulating hormone. 
  • EKG is necessary for all patients with suspected HF, and it helps rule out HF if completely normal, with a sensitivity of 89% but low specificity.[22] Abnormal EKG increases the likelihood of HF diagnosis.[23] It also can provide information on etiology (e.g., history of previous myocardial infarction makes CAD a possible cause of HF, arrhythmia as a potential cause of tachycardia-mediated cardiomyopathy HF, LV hypertrophy indicates hypertension-induced HF, widened QRS complex/left bundle branch block may suggest idiopathic dilated cardiomyopathy, and heart blocks as seen in patients with cardiac sarcoidosis) and provide indications for therapy (anticoagulation if atrial fibrillation, pacemaker in some bradycardia, and cardiac resynchronization therapy (CRT) if broadened QRS). 
  • Chest X-ray is also useful and may show pleural effusions secondary to volume overload, cardiomegaly, and Kerley B-lines (interstitial edema).
  • Transthoracic echocardiogram (TTE) is the most useful test that helps establish the diagnosis of HF and classify it as HFrEF, HFmrEF, or HFpEF. Abnormal parameters in HFrEF that can be measured by echocardiogram include increased end-diastolic diameter and volume (LV diameter over 60 mm or 32 mm/m with LV volume exceeding 97 mL/m) and end-systolic diameter and volume (LV diameter greater than 45 mm or 25 mm/m with LV volume over 43 mL/m).[24] Echocardiogram also helps to assess LVEF in HFrEF to guide evidence-based medical and device therapies (implantable cardioverter-defibrillator (ICD) and CRT), evaluate the valves, provide information on ventricular wall thickness, and it is vital in the risk stratification of patients with HF.[25]
  • Genetic testing: some CMP can be genetic, especially DCM, HCM, and autosomal dominant ARVD/C, and screening the family members may be important in family-based management. 
  • Computed tomography (CT) scanning or cardiac magnetic resonance imaging (cMR): neither are routinely indicated in the diagnosis and management of HF, and the role of imaging modalities other than TTE was restricted in the 2106 ESC guidelines. Cardiac CT can help to evaluate the coronary arteries in patients with HF with low to intermediate pretest probability of CAD. They provide information about cardiac function, have a high anatomical resolution of all aspects of the heart and surrounding structures (ventricular mass, chamber size, heart valves, and pericardium and wall motion).[26][27] Cardiac MRI assesses LV volume, LVEF, myocardial perfusion, viability, and fibrosis and helps identify HF etiology (ischemic versus non-ischemic disease, infiltrative disease, and hypertrophic disease) and assess prognosis. CMR can determine viability, help the success of revascularization in patients with low EF, and is the gold standard to evaluate the RV function. However, cMR is costly and cannot be performed with implantable defibrillators all the time (some of the defibrillators as MRI compatible these days). Also, both cardiac CT and cMR have low accuracy in patients with high heart rates. 
  • Left heart catheterization or coronary angiography is indicated in patients with HF and angina symptoms or ischemic changes by ECG or noninvasive testing. Indications also include worsening HF symptoms without a clear cause, when the pretest probability of underlying ICMP is high, before cardiac transplantation or LVAD, and in post-infarction mechanical complications like a ventricular aneurysm. It may be useful in patients with HF without angina but with LV dysfunction. In patients without CAD, CAD should be considered as a potential etiology of HF and impaired LV function and should be excluded whenever possible. It is only necessary if patients are potentially eligible for revascularization.[2]
  • Stress nuclear imaging or echocardiography may be an acceptable option for assessing ischemia in patients presenting with HF who have known CAD and no angina unless they are ineligible for revascularization. 


The diagnosis of HF is based on clinical signs and symptoms, laboratory workup, and echocardiogram. The Framingham clinical criteria help to diagnose (with low specificity) HF.[28] It includes major and minor criteria, and HF diagnosis requires two major or one major and two minor criteria. Major criteria include orthopnea, pulmonary rales, S3, cardiomegaly on chest X-ray, pulmonary edema on chest X-ray, elevated jugular venous pressure, paroxysmal nocturnal dyspnea, and weight loss over 4.5 kg in five days in response to treatment of presumed HF. Minor criteria include nocturnal cough, dyspnea on ordinary exertion, pleural effusion, hepatomegaly, tachycardia with a heart rate over 120 beats/min, bilateral leg edema, and weight loss under 4.5 kg in five days. However, Framingham's clinical criteria have excellent sensitivity to exclude the diagnosis of HF in the absence of these symptoms/signs, but it has poor specificity to confirm the diagnosis.[28] On the other hand, some patients with HF may not have symptoms. Only 50% of patients with LV dysfunction on an echocardiogram are symptomatic. Symptoms and signs of HF are either too nonspecific or too infrequent, which makes the clinical diagnosis of HF challenging with <25% of accuracy for most of the clinical features.

Measurement of natriuretic peptides (NPs) like BNP/NT-proBNP is also helpful in supporting the diagnosis in the ambulatory and inpatient settings. BNP has 70% sensitivity and 99% specificity for HF diagnosis, and NT-proBNP has 99% sensitivity and 85% specificity.[29] NPs have a very high negative predictive value of 0.94 to 0.98 and can exclude the diagnosis of HF (both HFpEF and HFrEF) if the values are below the cut-off. On the other hand, the positive predictive value of NPs is low (0.66 to 0.67) and cannot confirm the diagnosis.[30]


The cost-effectiveness of routine periodic population screening for asymptomatic reduced LVEF is not a current recommendation. Screening for hemochromatosis or HIV is reasonable in selected patients with HF (Class IIa, LOE: C).[2] Some genetic screening tests are also recommendations for HCM, idiopathic DCM, ARVC, isolated non-compaction CMP, and restrictive CMP.  

Treatment / Management

Treatment of HF starts from the prevention of overt HF by controlling the risk factors. Hypertension is a significant risk factor, and the cause of HF and intensive blood pressure control (systolic BP under 120 mmHg) was more beneficial for the prevention of cardiovascular diseases than standard treatment (systolic BP goal of less than 140 mmHg) in the SPRINT trial.[31] Recent studies have shown that sodium-glucose cotransporter-2 (SGLT-2) inhibitors reduced mortality and HF hospitalization in patients with type 2 diabetes.[32] In patients with STEMI, rapid primary percutaneous coronary intervention (PCI) and administration of ACEI, beta-blocker, mineralocorticoid receptor antagonists (MRAs), and statin can reduce HF hospitalization and mortality.

Treatment of HF is indicated in all patients with LV dysfunction (diastolic or systolic) regardless of symptoms. The goal of treatment is to improve survival and symptoms, reduce the length of stay and HF readmission, decrease morbidity, prevent organ damage from HF, and prevent symptoms in asymptomatic LV dysfunction. Treatment of HF can fall into non-pharmacological therapy, pharmacological therapy, devices and non-surgical interventions, and invasive strategies. 

  • Nonpharmacological therapy

Non-pharmacological therapy is indicated for all types of HF regardless of EF. It is consistent with behavioral and lifestyle modifications including dietary and nutritional consultation (sodium restriction to 2 to 3 g/day, fluid restriction to 2 L/day if there is hyponatremia, and caloric supplementations if cardiac cachexia), strict adherence to therapy and diet, daily weight and diuretic dosing adjustment for sudden weight changes, patient education to facilitate self-care/close observation/follow up, aerobic exercise training (can reverse LV remodeling in stable patients), controlling of HBP, DM and lipid disorders, and smoking/alcohol/illicit drug use cessation.

  • Pharmacologic therapy for HFrEF

Initial pharmacologic therapy includes a combination of diuretics (as needed for volume overload to improve symptoms but they do not improve survival and routine use of loop diuretics without volume overload signs or symptoms may even increase mortality [33]), an angiotensin system blocker (ACEi, ARB, or ARNI) or hydralazine plus nitrate as an alternative if no tolerance to angiotensin system blockers, and a beta-blocker. Other medications that are options in selected patients are MRA, ivabradine, and digoxin. 

1- ACEi or ARBs (class IA) are the first-line therapies, and the dose should titrate up to the maximum tolerated evidence-based doses. ACEis inhibit the activity of angiotensin-converting enzyme (ACE) and therefore prevent the formation of angiotensin II from angiotensin I, and that causes natriuresis, diuresis, and a reduction in arterial blood pressure and thereby afterload. ACEIs have been in use for many years, and multiple clinical trials have shown survival benefits and decrease hospitalization in chronic symptomatic HFrEF as in the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS) and the Studies of Left Ventricular Dysfunction (SOLVD).[34][35] ARBs have not consistently proven to reduce mortality in patients with HFrEF, and their use should be restricted to patients intolerant of an ACEI. According to the current ESC and AHA/ACCF guidelines, every patient with HFrEF should receive an ACEI independent of symptoms and if no contraindications. This group includes captopril, lisinopril, ramipril, enalapril, quinapril, losartan, valsartan, irbesartan, and candesartan. The routine combination of ACEi, ARB, and MRA is not recommended and may cause more symptomatic hypotension and worsening renal function (class III C). 

Angiotensin receptor-neprilysin inhibitor (ARNI) sacubitril/valsartan was approved by FAD in 2015 for HFrEF treatment after the Prospective Comparison of ARNI with ACE-I to Determine Impact on Global Mortality and Morbidity in Heart Failure (PARADIGM-HF) trial in 2014 that found a markedly decreased cardiovascular and all-cause mortality in patients with HFrEF in the sacubitril/valsartan group compared to enalapril.[36] It is indicated in patients with symptomatic HFrEF with EF ≤40%, elevated plasma NP levels (BNP ≥150 pg/mL or NT-proBNP ≥600 pg/mL or, if they had been hospitalized for HF within the previous 12 months, BNP ≥100 pg/mL or NT-proBNP ≥400 pg/mL), and an estimated GFR (eGFR) ≥30 mL/min/1.73 m of body surface area as per the ESC 2016 guidelines.[37] Sacubitril/valsartan has some safety issues, and long-term safety is a concern. It can cause more symptomatic hypotension, especially in the elderly, and had more angioedema cases than enalapril in the PARADIGM-HF trial. To minimize the angioedema risk caused by overlapping ACE and neprilysin inhibition, the clinicians should withhold the ACEi for at least 36 hours before initiating the sacubitril/valsartan. In a recent meta-analysis, ARNI improved LVH, LV size, and reverse cardiac remodeling compared with ACEi/ARBs in patients with HFrEF and caused marked changes in the left ventricular mass index and left atrial volume in HFpEF.[38][38] 

2- Beta Blockers (Class IB): one of the pathophysiologies of HFrEF is ongoing sympathetic activation that adversely affects the cardiac myocytes and contractility, so blocking this pathway with beta-blockers reverses this mechanism and help improve HFrEF. Beta-Blockers improve survival, reduce HF hospitalizations, and increase LVEF in chronic HFrEF.[39] Several studies have shown the benefits of beta-blockers on survival, including the Study of the Effects of Nebivolol Intervention on Outcomes and Re-hospitalization in Seniors with Heart Failure (SENIORS) and Carvedilol Prospective Randomized Cumulative Survival (COPERNICUS), among many other studies.[40] Randomized controlled trials support carvedilol, metoprolol succinate, and bisoprolol. According to the current ESC guidelines, ACEIs and beta-blockers should be started immediately after the diagnosis of HFrEF.[41]   

3- Mineralocorticoid Receptor Antagonists (MRAs): the class IA indication for MRAs as per the 2013 ACCF/AHA guidelines is in patients with NYHA class II-IV who have EF of 35% or less, serum creatinine less than 2 .5 mg/dL, or an estimated glomerular filtration rate over 30 mL/min/1.73 m, and stable serum potassium less than 5.0 mEq/L at the initiation of therapy. MRAs also decrease mortality and hospitalization in chronic HFrEF (NYHA class II-IV). However, a meta-analysis of 1575 patients enrolled in 14 studies reported an improvement in LVEF of 3.2% and a significant improvement in NYHA class among subjects treated with aldosterone antagonists (p<0.001) regardless of baseline LVEF or NYHA class.[42] 

4- Nitrates Plus Hydralazine: they both decrease afterload, and nitrates also reduce the preload. According to the 2013 ACCF/AHA guidelines, it is a Class IA indication that decreases mortality and morbidity in HFrEF among African Americans with NYHA class III-IV HF receiving optimal medical therapy (OMT) with ACEi and beta-blockers. 

5- Digoxin: it can decrease hospitalization of HFrEF (class IIA, level of evidence B), but it does not improve survival. Some evidence suggests that digoxin increases mortality in women but not in men; its use requires caution in women with symptomatic heart failure.[43]  

6- Aspirin and statin for ischemic HF. 

7- Ivabradine was approved by FAD in 2015 to reduce the risk of HF hospitalization. It is indicated in stable, symptomatic patients with chronic HFrEF with EF under 35%, who are in sinus rhythm and demonstrate a resting heart rate exceeding 70 bpm on the maximum tolerated dose of beta-blocker or have contraindications for beta-blockers.[44]

8- Sodium-glucose cotransporter 2 inhibitor: in patients with HFrEF who still have symptoms and elevated BNP levels on optimal medical therapy (OMT) and device therapy, the recommendation is to add dapagliflozin (versus no additional drug therapy) (grade 1 B) even in patients without DM as shown by the DAPA-HF Trial.[45] It is contraindicated in patients with symptomatic hypotension, SBP under 95 mmHg, eGFR below 30 ml per minute per 1.73 m

9- Continuous intravenous inotrope (dobutamine or milrinone) is reasonable as bridge therapy for cardiac transplantation or Ventricular Assist Devices (VADs) in patients with stage D HF refractory to Guideline Directed Medical Therapy (GDMT) (class IIa, LOE:B) or as a palliative care as per the 2013 ACCF/AHA guidelines. 

  • Medications to avoid in HF

According to the ESC guidelines, some treatments can be harmful in patients with HF and should be avoided[37]: 

1- Non-steroidal anti-inflammatory drugs (NSAIDs), COX-2 inhibitors: they can worsen HF, increase hospitalization, worsen kidney functions, and cause more sodium and water retention.[46]

2- Calcium Channel Blockers (CCB) excluding amlodipine and felodipine: [47] they have negative inotropic effects and may worsen HF and increase hospitalizations.

3- Thiazolidinediones (TZDs): can cause fluid extension and exacerbate an existing HF and increase the risk of HF in patients without HF. The benefit/risk profile of TZDsmerit consideration when treating DM in patients with or without prior HF.[48]

4- Adding an ARB to an ACEi and an MRA possibly will worsen kidney function and increase the risk of hyperkalemia.

5- Dronedarone should not be an option in patients with NYHA class III-IV HFrEF as per ANDROMEDA (antiarrhythmic trial with dronedarone in moderate to severe CHF evaluating morbidity decrease study). Dronedarone also demonstrated worse cardiovascular outcomes in patients with HFpEF.[49]

Other medications that should be avoided or at least used with caution in patients with HF are metformin (increase the risk of potentially lethal lactic acidosis), phosphodiesterase inhibitor (PDE-3 inhibitors increased mortality, PDE-5 inhibitors are harmful in patients with HF who have borderline low BP and/or low volume status), antiarrhythmic agents (especially class I and III) due to negative inotrope activity (amiodarone is the preferred drug for the treatment of arrhythmias in patients with HF.  

  • Devices and non-surgical interventions

These include implantable cardioverter-defibrillator (ICD) and cardiac resynchronization therapy (CRT). Before proceeding with device therapy, patients should be treated with ACEi/ARB plus Beta-blockers for at least three months and then reassess the LVEF. If EF remains less than or equal to 35%, the recommendation is a referral for device therapy. 


ACC/AHA 2013 guidelines [2] recommend ICD for primary prevention of sudden cardiac death for non-ischemic dilated cardiomyopathy (NIDCM) or ischemic CMP (ICM) at least 40 days post-MI on chronic goal-directed medical therapy (GDMT) with either LVEF ≤ 35% and NYHA class II or III symptom (I-A) or LVEF ≤ 30% and NYHA class I symptom (I-B) 

ESC 2016 guidelines [1] recommend ICD for primary prevention in symptomatic HF (NYHA II-III) with LVEF ≤ 35% despite ≥ three months of GDMT in ICM (IA) or NIDCM (IB)


ACC/AHA 2013 guidelines recommend CRT for patients with HF with sinus rhythm, LVEF ≤ 35%, left bundle branch block (LBBB) with QRS duration ≥ 150 ms, and NYHA class III (I-A) or ambulatory IV (I-A) or II (I-B) on GDMT. 

ESC 2016 guidelines recommend CRT for symptomatic HF with sinus rhythm and LVEF ≤ 35% despite GDMT with LBBB with QRSd ≥ 150 ms (I-A) or 130 to 149 ms (I-B). 

Coronary revascularization (Coronary Artery Bypass Grafting or CABG, angioplasty, and Percutaneous Coronary Intervention or PCI) is indicated for patients with HF (HFpEF, HFrEF, or HFmrEF) on GDMT with angina and suitable coronary anatomy (class IC). 

Despite the advances in the medical management of HF, there are some circumstances in which surgery is the best treatment option. Surgical approaches to HF treatment include heart transplantation and procedures that reshape the heart, repair the heart, or replace all or part of the heart function. The basis for any decision to surgically treat HF depends on functional status, prognosis, and severity of the underlying HF and comorbidities. It should take place in centers with multidisciplinary medical and surgical teams.  

Heart Transplantation

According to Heart Failure Society of America (HFSA) 2010 heart failure guidelines, it is recommended to evaluate patients for heart transplantation in severe HF, debilitating refractory symptoms, ventricular arrhythmia, or congenital heart disease that remains uncontrolled despite drug, device, or alternative surgical therapy (strength of evidence B).[50] Data of the registry of the International Society of Heart and Lung Transplantation indicates a current 1-year survival of 84.5% and 5-year survival of 72.5%; subsequently, survival decreases linearly by approximately 3.4% per year.[51]

Ventricular Assist Devices (VADs)

The blood is removed from the failing ventricle and diverted into a pump that delivers the blood to either the aorta (in case of LV failure and LVAD) or the pulmonary artery (in case of right ventricle failure and RVAD). Devices for this process include left ventricular assist device (LVAD), right ventricular assist device (RVAD), or biventricular assist devices (BiVAD), and Impella device, which is inserted percutaneously into the LV and draws blood from LV and expels it into the ascending aorta. This VADs are used as a bridge therapy to heart transplantation in refractory stage D heart failure according to the ACCF/AHA, ESC, and HFSA guidelines, or as a destination therapy if not a candidate for heart transplantation as LVADs as destination therapy, in this case, is superior to medical therapy according to the Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure (REMATCH) trial.[2][37][50][51][52]

Surgical Ventricular Restoration (SVR)

One of the mechanisms of HF pathophysiology is ventricular remodeling and the shape change from an elliptical shape to a spherical shape, especially post transmural MI. Correction of this pathologic remodeling by incising and excluding the nonviable myocardium with either patch or primary reconstruction to decrease the ventricular volume may be hypothetically helpful in treating patients with HF. However, the STICH trial, which is the major study for ventricular reconstruction, found that adding ventricular surgical reconstruction to CABG reduced the left ventricular volume, as compared with CABG alone, but this did not correlate with a greater improvement in symptoms or exercise tolerance or with a reduction in the mortality rate or hospitalization for cardiac causes.[53] SVR is not routinely recommended and is not in the ESC, AHA/ACCF, or HFAS guidelines. 

Treatment of HFpEF and HFmrEF

There are no disease-modifying therapies for HFpEF or HFmrEF that improve outcomes comparing to HFrEF agents. Efficacious therapies for HFrEF have failed to demonstrate a benefit for HFpEF, and more research is required to evaluate them in HFmrEF.[1] Spironolactone has been shown to reduce HF hospitalization rates in HFpEF, but no treatment has demonstrates improved survival.[54] Treatment focuses on controlling BP using beta-blockers, ACEi or ARBs is reasonable to control BP in patients with HFpEF (class IIA), diuretics to relieve symptoms of volume overload, and to address the risk factors and comorbidities. There are no studies to determine the impact of revascularization on symptoms or outcomes, specifically in patients with HFpEF. It might be reasonable to consider revascularization in patients for whom ischemia appears to contribute to HF symptoms.

Treatment of Right Heart Failure

The most frequent causes of RV failure are LV failure and primary pulmonary diseases, and treating the underlying cause is essential in RV failure treatment. ACEi/ARB and beta-blockers' efficacy in isolated RV failure is not known, but they are beneficial if RV failure is secondary to LV failure. If severe unstable RV failure, the use of inotrope may be a consideration. The prognosis in patients with RV failure depends on the etiology. Volume overload, pulmonary stenosis, and Eisenmenger syndrome are associated with a better prognosis. Decreased exercise tolerance predicts poor survival. 

Treatment of acute decompensated heart failure (ADHF) 

Diagnosis of ADHF is based on symptoms and signs with the help of BNP, NT-proBNP concentration if the clinical diagnosis is uncertain. Hospitalization is necessary if severely decompensated HF (hypotension, worsening renal function, or altered mentation), dyspnea at rest, hemodynamically significant arrhythmia (including new-onset rapid atrial fibrillation), or acute coronary syndromes. Successful inpatient therapy for ADHF involves a comprehensive care plan. Etiology and precipitating factors require identification, chronic oral therapy should be optimized, treatment to relieve symptoms should be applied (loop intravenous diuretics or ultrafiltration if diuretic resistance, and vasodilators to decrease preload and afterload), the patient that may benefit from revascularization or device therapies should be identified, education about dietary sodium restriction/self-assessment of volume status and principal cardiac medications should be provided. The use of non-invasive positive pressure ventilation may be useful in severely dyspneic patients with evidence of pulmonary edema. The cornerstone of ADHF is volume removal. Loop diuretics (furosemide, torsemide, or bumetanide) are the preferred initial diuretics, and if inadequate diuresis, a second diuretic can be added (e.g., a thiazide). Vasodilators (nitroprusside, nesiritide, or nitroglycerin) are also recommended as an adjuvant to diuresis to relieve symptoms but should be avoided if systolic BP less than 90 mmHg or in cases of significant aortic or mitral stenosis.[1] ACEi/ARBs and Beta-blockers should be continued during the HF exacerbation in HFrEF if no contraindication (in patients with significant worsening renal function, the clinician can temporarily discontinue ACEi/ARBs and/or MRA until renal function improves. Most patients will tolerate continuing the beta-blockers well, but this can be held if marked volume overload or marginal/low CO. Medical treatment should be optimized. If the patient is not on ACEi/ARB/ARNI or beta-blockers, those should be started when feasible while inpatient.

Differential Diagnosis

The diagnosis of HF is mostly clinically, as mentioned above, but many other medical conditions can cause the same signs and symptoms. There is a broad differential diagnosis of HF, which includes but is not limited to bacterial pneumonia, chronic obstructive pulmonary disease (COPD), liver cirrhosis, acute kidney injury, idiopathic pulmonary fibrosis, nephrotic syndrome, pulmonary embolism respiratory failure, primary pulmonary hypertension, anemia, and venous insufficiency.

  • Acute kidney injury
  • Bacterial pneumonia
  • Acute respiratory distress syndrome
  • Cardiogenic pulmonary edema
  • Interstitial (non-idiopathic) pulmonary fibrosis
  • Chronic obstructive pulmonary disease
  • Cirrhosis
  • Goodpasture syndrome
  • Community-acquired pneumonia
  • Idiopathic pulmonary fibrosis
  • Myocardial infarction
  • Pulmonary embolism
  • Nephrotic syndrome
  • Neurogenic pulmonary edema
  • Pneumothorax
  • Respiratory failure
  • Viral pneumonia
  • Venous insufficiency


Heart failure divides into four stages, according to the 2013 ACCF/AHA Guidelines [55]: 

Stage A- At high risk for HF but no structural heart disease or symptoms of HF

Stage B- Asymptomatic LV dysfunction: structural heart disease but no symptoms or signs of HF 

Stage C- Overt HF: structural heart disease with symptoms of HF 

Stage D- Refractory HF. 

Symptoms of HF are only in stages C and D.


New York Heart Association ( NYHA) classifies HF based on HF symptoms and functional limitations into four classes[56]:

Class I: asymptomatic LV dysfunction with no limitations on physical activity or symptoms. 

Class II: mild symptoms with slight limitation of physical activity. Ordinary activities lead to symptoms.

Class III: moderate symptoms with marked limitation of physical activity. Less than ordinary activities lead to symptoms.

Class IV: severe symptoms at rest.


Changes in EF over time are more prognostic of HF than baseline EF. Patients who progress from HFmrEF to HFrEF have a worse prognosis than those who progress to HFpEF or remain stable in HFmrEF. The mortality rate is higher in HFrEF than HFmrEF and HFpEF, according to OPTIMIZE-HF trail [57] that showed a mortality rate of 3.9% for HFrEF, 3% for HFmrEF, and 2.9% for HFpEF. The mortality rate is also higher in symptomatic patients. There are some predictors of poor prognosis and increased mortality in hospitalized patients, which include systolic blood pressure less than 115 mmHg, serum creatinine greater than 2.7 mg/dL, serum urea over15 mmol/L, NT-pro-BNP exceeding 986 pg/mL, and LVEF under 45%.[58] Poor prognostic factors in chronic heart failure include S3 gallop, DM, hyponatremia, decreased LVEF, high NYHA functional class, reduced cardiac index, and increased pulmonary artery capillary wedge pressure.[59]


HF may cause multiple complications, including but not limited to:

  • Arrhythmias: Atrial fibrillation (Afib) can be a cause or a consequence of HF and may present in 10% to 50% of chronic HF patients, and those patients with HF and Afib have a poor prognosis. Malignant ventricular arrhythmias (like sustained monomorphic ventricular tachycardia, sustained polymorphic ventricular tachycardia, and torsades de pointes) are common in end-stage heart failure, especially if precipitating or factors are present like electrolyte disturbance, prolonged QT interval, and digoxin toxicity. Bradyarrhythmias may also happen.[60]
  • Thromboembolism: HF is a cause of stroke in 9% of patients.[61] Between 10 and 24% of patients with stroke have HF.[62][63] There is a high relative risk for deep venous thrombosis (DVT) and pulmonary embolism (PE) in patients with HF, especially those who were under 60 years of age.[64]
  • Gastrointestinal: liver shock (ischemic hepatitis), liver cirrhosis, and cardiac cachexia due to decreases intestinal blood flow in patients with HF.[65] 
  • Renal: renal function may get worse in both acute and chronic HF, and that predicts poor prognosis, and even a small transient rise in creatinine will be clinically relevant.[66]
  • Respiratory: pulmonary congestion, respiratory muscle weakness, and rarely pulmonary hypertension 

Deterrence and Patient Education

Emphasizing diet and medical compliance to patients with HF is important as one of the most common causes of HF readmission is the failure to comply either with diet or medications. A single session intervention could be beneficial as a randomized control trial of 605 patients with HF found that the incidence of all-cause hospitalization or mortality was not significantly reduced in patients receiving multisession self-care training compared to those receiving a single-session intervention.[67]

Enhancing Healthcare Team Outcomes

Heart failure is a leading cause of hospitalization and represents a significant clinical and economic burden. The long-term goal of treatment is to avoid exacerbation of HF and decrease hospital readmission rates. It needs an interprofessional approach involving patients, physicians, nurses, pharmacists, families, and caretakers. Those strategies include early identification of high-risk patients, patient education, improving medication and dietary compliance, assuring close follow up, introducing end-of-care issues, and tele-home monitoring if available. Primary care and emergency department providers often are the first to make this diagnosis. Referal to cardiologists is often appropriate. Cardiology, medical/surgical, and critical care nurses administer treatment, provide education, monitor patients, and communicate with the rest of the team so that everyone on the healthcare team operates from the same data set. The managing clinician would do well to consult with a board-certified cardiology pharmacist when initiating pharmaceutical care in HF cases. Pharmacists also review medicines, check the dosages, detect drug-drug interactions, and stress to patients and their families the importance of compliance. In end-stage cases, hospice care and hospice nurses can work with the patient and their family to provide comfort care. These interprofessional collaborations will optimize patient outcomes in HF cases. [Level 5]

(Click Image to Enlarge)
 The illustration shows the major signs and symptoms of heart failure.
The illustration shows the major signs and symptoms of heart failure.
Contributed by National Heart, Lung, and Blood Institute, National Institutes of Health (NIH)

(Click Image to Enlarge)
NYHA Classification - Heart failure
NYHA Classification - Heart failure
Contributed by the New York Health Association (NYHA)

(Click Image to Enlarge)
Frank-Starling Curve
Frank-Starling Curve
Contributed by Said Hajouli



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Acute heart failure

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None of the individuals in control of the content for this article (a continuing medical education activity) reported relevant financial relationships with commercial interests.

The full conflict of interest (COI) policy for our continuing medical education (CME) program can be found within “AMBOSS CME information and policies.”

Summarytoggle arrow icon

Acute heart failure is the rapid onset or worsening of heart failure symptoms, and it is a common cause of hospitalization in older patients. Multiple triggers can cause an acute decompensation of preexisting heart failure (ADHF) but the condition may also occur suddenly in patients with no previous history of the condition (de novo heart failure). Diagnosis is based on typical clinical features (e.g., dyspnea), laboratory findings (e.g., elevated BNP), and imaging findings (e.g., pulmonary edema). Management is often challenging because of comorbidities; most patients require admission for treatment with IV diuretics, vasodilators, adjustment of their chronic heart failure medications, respiratory support, and careful monitoring.

Definitiontoggle arrow icon

Etiologytoggle arrow icon

Pathophysiologytoggle arrow icon

Clinical featurestoggle arrow icon

Clinical features of acute heart failure are commonly classified according to perfusion and the presence of congestion at rest. [1][2][5]

Classification of acute heart failure[5][6]
No evidence of congestion (∼5% of patients) Evidence of congestion (∼95% of patients)
Adequate perfusion
  • Congestion (most common) [1]
  • Hypoperfusion

Diagnosticstoggle arrow icon

Diagnosis of acute heart failure consists of a combination of clinical features, laboratory markers (e.g., BNP), and supportive imaging findings. It is important to evaluate for the underlying cause and rule out life-threatening comorbidities (e.g., ACS).

Laboratory studies[7]

  • ↑ BNP (or NT-proBNP): Measure in every patient suspected of having acute heart failure.
    • Should always be interpreted in comparison to the patient's baseline and in the context of history, examination, and imaging.
    • High diagnostic utility in patients with unclear diagnosis [7]

Measuring BNP (or NT-proBNP) is especially helpful in patients with unclear diagnosis. BNP has a high diagnostic value when combined with physical examination and imaging.


Indicated in all patients to exclude ACS. Findings are variable and may include: [5][6]

Initial imaging

All patients with suspected acute heart failure should have a CXR and echocardiography performed.


ABCDE: Alveolar edema (bat wings), Kerley B lines (interstitialedema), Cardiomegaly, Dilated prominent pulmonary vessels, and Effusions

Transthoracic echocardiogram (TTE) [5][17]

POCUS in acute heart failure

Advanced imaging

If more detailed information about myocardial viability and/or perfusion is needed (e.g., procedural planning, myocardialischemia is suspected), further imaging modalities may be necessary after the patient is stabilized. Both MRI and CT require the patient to lie flat for sustained periods and are less accurate at higher heart rates.

Differential diagnosestoggle arrow icon

See also “Differential diagnoses of dyspnea.”

The differential diagnoses listed here are not exhaustive.

Managementtoggle arrow icon

Approach [6]

Hemodynamically unstable patients (i.e., cardiogenic shock) [6][25]

See “Management of cardiogenic shock” for details on therapeutic targets and monitoring. See “Treatment of refractory AHF” for management of patients with cardiogenic shock refractory to the following interventions.

Avoid inotropes in patients with left ventricular outflow tract obstruction (e.g., hypertrophic cardiomyopathy, aortic stenosis). [28]

Hemodynamically stable patients

Respiratory support in acute heart failure[6]

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Treatment of Congestive Heart Failure (CHF)

Congestive heart failure

Summarytoggle arrow icon

Congestive heart failure (CHF) is a clinical condition in which the heart is unable to pump enough blood to meet the metabolic needs of the body because of pathological changes in the myocardium. The three main causes of CHF are coronary artery disease, diabetes mellitus, and hypertension. These conditions cause ventricular dysfunction with low cardiac output, which results in blood congestion and poor systemic perfusion. CHF is classified as either left heart failure (LHF) or right heart failure (RHF), while a combination of both is called biventricular or global CHF. LHF leads to pulmonary edema and consequent dyspnea, while RHF leads to systemic venous congestion that causes symptoms such as pitting edema, jugular venous distension, and hepatomegaly. Biventricular CHF manifests with clinical features of both RHF and LHF, as well as general symptoms such as tachycardia, fatigue, and nocturia. In rare cases, high-output CHF may occur as a result of conditions that increase metabolic demands, leading to an increased cardiac output that eventually overwhelms the heart. CHF is diagnosed based on clinical presentation and requires an initial workup to assess the severity of the disease and determine the possible causes. Initial workup includes measurement of brain natriuretic peptide levels, chest x-ray, ECG, and an echocardiogram. Management of CHF includes lifestyle modifications and treatment of associated conditions (e.g., hypertension) and comorbidities (e.g., anemia), along with pharmacological agents that reduce the workload of the heart. Acute heart failure may occur as an exacerbation of CHF (acute decompensated heart failure) or be caused by an acute cardiac condition such as myocardial infarction (see “Acute heart failure”).

Definitiontoggle arrow icon

  • Heart failure (HF): a complex of signs and symptoms caused by structural or functional impairment of ventricular filling and/or ejection of blood [1]
  • Congestive heart failure (CHF): a clinical syndrome in which the heart is unable to pump enough blood to meet the metabolic needs of the body
  • Heart failure with reduced ejection fraction (HFrEF, systolic HF): CHF with reduced stroke volume, reducedejection fraction (EF) (left ventricular EF ≤ 35–40%)
  • Heart failure with preserved ejection fraction (HFpEF, diastolic HF): CHF with reduced stroke volume, normal/reduced EDV, and preserved EF (LVEF≥ 40–50%)
  • Right heart failure (RHF): CHF due to right ventricular dysfunction resulting in congestion of blood in the vena cavae and peripheral veins, which increases venous hydrostatic pressure and results in peripheral edema, increased jugular venous pressure, ascites, and hepatomegaly.
  • Left heart failure (LHF): CHF due to left ventricular dysfunction resulting in tissue hypoperfusion and increased pulmonary capillary pressure
  • Biventricular (global) CHF: CHF in which both the left and right ventricles are affected resulting in the development of both RHF and LHF symptoms
  • Chronic compensated CHF: a patient has signs of CHF on echocardiography but is asymptomatic or symptomatic and stable [2]
  • Acute decompensated CHF: sudden deterioration of CHF or new onset of severe CHF due to an acute cardiac condition (e.g., myocardial infarction)

Epidemiologytoggle arrow icon

  • ∼ 1.9% of the population in the US has CHF (∼ 6.2 million individuals) [3]
  • The incidence is higher among African Americans and Hispanics. [4]
  • Incidence increases with age: ∼ 10% of individuals > 60 years old are affected.[5]
  • Systolicheart disease is the most common form of CHF overall.

Epidemiological data refers to the US, unless otherwise specified.

Etiologytoggle arrow icon

The three major causes of heart failure are coronary artery disease, hypertension, and diabetes mellitus. Patients typically have multiple risk factors that contribute to the development of CHF.

Classificationtoggle arrow icon

American Heart Association (AHA) classification (2013) [1]

The AHA classification system categorizes patients according to the stage of disease based on an objective assessment of clinical features and diagnostic findings.

StagesObjective assessmentCorresponding NYHA functional class
Stage A
Stage B
Stage C
Stage D
  • Terminal stage heart failure

NYHA functional classification[1]

The NYHA (New York Heart Association) functional classification system is used to assess the patient's functional capacities (i.e., limitations of physical activity and symptoms) and has prognostic value.

NYHA classCharacteristics
Class I
  • No limitations of physical activity
  • No symptoms of CHF
Class II
  • Slight limitations of moderate or prolonged physical activity (e.g., symptoms after climbing 2 flights of stairs or heavy lifting)
  • Comfortable at rest
Class III
  • Marked limitations of physical activity (e.g., symptoms during daily activities like dressing, walking across rooms)
  • Comfortable only at rest
Class IV
  • Confined to bed, discomfort during any form of physical activity
  • Symptoms at rest

Pathophysiologytoggle arrow icon

Cardiac output, which is stroke volume times heart rate, is determined by three factors: preload, afterload, and ventricular contractility.

Underlying mechanism of reduced cardiac output

  • Heart failure with reduced ejection fraction (HFrEF)
  • Heart failure with preserved ejection fraction (HFpEF)
  • Left-sided heart failure (HFrEF and/or HFpEF)
  • Right-sided heart failure

Consequences of decompensated heart failure

CHF is characterized by reduced cardiac output that results in venous congestion and poor systemic perfusion.

Compensation mechanisms

The compensation mechanisms are meant to maintain the cardiac output when stroke volume is reduced.

Clinical featurestoggle arrow icon

General features of heart failure

Clinical features of left-sided heart failure

Clinical features of right-sided heart failure

Sours: https://www.amboss.com/us/knowledge/Congestive_heart_failure/

Failure usmle heart

Heart Failure With Preserved Ejection Fraction (Diastolic Heart Failure)

Topic Overview

Heart failure with preserved ejection fraction (HFpEF) occurs when the lower left chamber (left ventricle) is not able to fill properly with blood during the diastolic (filling) phase. The amount of blood pumped out to the body is less than normal.

It is also called diastolic heart failure.

What does preserved ejection fraction mean?

The types of heart failure are based on a measurement called the ejection fraction. The ejection fraction measures how much blood inside the ventricle is pumped out with each contraction. The left ventricle squeezes and pumps some (but not all) of the blood in the ventricle out to your body. A normal ejection fraction is more than 55%. This means that 55% of the total blood in the left ventricle is pumped out with each heartbeat.

Heart failure with preserved ejection fraction (HFpEF) happens when the left ventricle is not filling with blood as well as normal. The ventricle can pump well. But it may be stiff so it cannot relax and fill with blood as well as normal. The ejection fraction is 50% or more. HFpEF may also be diagnosed if the ejection fraction is 40% to 49%.footnote 1

Although the ejection fraction may be normal, the heart has less blood inside it to pump out. So the heart pumps out less blood than the body needs.

Examples of ejection fractions of a healthy heart and a heart with preserved ejection fraction:

  • A healthy heart with a total blood volume of 100 mL that pumps 60 mL has an ejection fraction of 60%.
  • A heart with a stiff left ventricle that has a total blood volume of 90 mL and pumps 50 mL has an ejection fraction of 55%.

HFpEF happens because the left ventricle's muscle becomes too stiff or thickened. To compensate for stiff heart muscle, your heart has to increase the pressure inside the ventricle to properly fill the ventricle. Over time, this increased filling causes blood to build up inside the left atrium and eventually into the lungs, which leads to fluid congestion and the symptoms of heart failure.

What causes it?

The most common cause of diastolic heart failure is the natural effect of aging on the heart. As you age, your heart muscle tends to stiffen, which can prevent your heart from filling with blood properly, leading to diastolic heart failure.

But there are many health problems that can impair your left ventricle's ability to fill properly with blood during diastole.


What is it?

How it causes heart failure

Coronary artery disease (CAD)

Blockage of the arteries that supply blood to the heart

Low blood flow to the heart muscle (ischemia) can prevent the heart from relaxing and filling with blood.

High blood pressure

Elevated pressure in your arteries

Heart muscle can thicken the wall of the heart (hypertrophy) in an effort to pump against high blood pressure. Thickened heart muscle limits the heart's ability to relax and fill with blood.

Aortic stenosis

Narrowed opening of the aortic valve

The left ventricle thickens, limiting its ability to fill.

Hypertrophic cardiomyopathy

Inherited abnormality of heart muscle resulting in very thick walls of the left ventricle

Thick heart muscle prevents blood from filling the left ventricle.

Pericardial disease

Abnormality of the sac that surrounds the heart (pericardium)

Fluid in the pericardial space (pericardial tamponade) or a thickened pericardium (pericardial constriction) can limit the heart's ability to fill.



  1. Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management of heart failure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147–e239.

Other Works Consulted

  • Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management of heart failure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147–e239.
  • Zile MR, Little WC (2015). Heart failure with a preserved ejection fraction. In DL Mann et al., eds., Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 10th ed., vol. 1, pp. 557–574. Philadelphia: Saunders.


Current as of: August 31, 2020

Author: Healthwise Staff
Medical Review:
Rakesh K. Pai MD, FACC - Cardiology, Electrophysiology
E. Gregory Thompson MD - Internal Medicine
Martin J. Gabica MD - Family Medicine
Adam Husney MD - Family Medicine
Stephen Fort MD, MRCP, FRCPC - Interventional Cardiology

Sours: https://www.uofmhealth.org/health-library/tx4091abc
Congestive Heart Failure - HFrEF \u0026 HFpEF *USMLE STEPS 2 \u0026 3*

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